中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (20): 3789-3792.doi: 10.3969/j.issn.1673-8225.2011.20.044

• 组织构建细胞学实验 cytology experiments in tissue construction • 上一篇    下一篇

周期性张应力诱导成纤维细胞凋亡中p38MAPK信号通路的作用

仇  静1,张广耘2,田  臻1,张  月2,于江波2,袁  晓2   

  1. 1青岛大学医学院附属医院青岛市立医疗集团口腔科,山东省青岛市  266000
    2 青岛市市立医疗集团口腔科,山东省青岛市  266071
  • 收稿日期:2011-01-19 修回日期:2011-03-23 出版日期:2011-05-14 发布日期:2011-05-14
  • 通讯作者: 张广耘,硕士,教授,青岛市市立医疗集团口腔科,山东省青岛市 266071
  • 作者简介:仇静★,女,1985年生,山东省青岛市人,汉族,青岛大学在读硕士,主要从事牙周病学研究。
  • 基金资助:

    国家自然科学基金(30871426),课题名称:p38MAPK信号通路在周期性张应力诱导的成纤维细胞凋亡中的作用。

Effects of p38MAPK signaling pathway on cyclic tensile stress-induced fibroblast apoptosis

Qiu Jing1, Zhang Guang-yun2, Tian Zhen1, Zhang Yue2, Yu Jiang-bo2, Yuan Xiao2   

  1. 1Department of Stomatology, Qingdao Municipal Hospital (Oral), the Affiliated Hospital of Medical College, Qingdao University, Qingdao  266000, Shandong Province, China
    2Department of Stomatology, Qingdao Municipal Hospital (Oral), Qingdao  266071, Shandong Province, China
  • Received:2011-01-19 Revised:2011-03-23 Online:2011-05-14 Published:2011-05-14
  • Contact: Zhang Guang-yun, Master, Professor, Department of Stomatology, Qingdao Municipal Hospital (Oral), Qingdao 266071, Shandong Province, China zhanggyqd@126. com
  • About author:Qiu Jing★, Studying for master’s degree, Department of Stomatology, Qingdao Municipal Hospital (Oral), The Affiliated Hospital of Medical College, Qingdao University, Qingdao 266000, Shandong Province, China hi.andy1985@163. com
  • Supported by:

    the National Natural Science Foundation of China, No. 30871426*

摘要:

背景:当牙齿受异常咬合力时会导致牙体吸收、牙周组织的大量破坏。
目的:研究牙周膜成纤维细胞在受到周期性张应力刺激后是否发生凋亡及p38MAPK信号通路是否参与该凋亡过程。
方法:取4~7代成纤维细胞,同步化后随机分为对照组、加力组和SB203580组。加力组和SB203580组细胞加载力值为12%表面应变率,加力频率为6个循环/min,即5 s拉伸,5 s松弛。SB203580组细胞在加力前1 h加入终浓度为20 mmol/L的p38MAPK抑制剂SB203580。分别在加力6,12,24 h,取各组细胞,流式细胞仪检测细胞凋亡,RT-PCR检测细胞凋亡基因bax mRNA的表达。
结果与结论:与对照组比较,加力后成纤维细胞凋亡率及bax mRNA表达增加 (P < 0.05),且随着加力时间的延长而增强,12 h达高峰,之后逐渐下降。与加力组比较,SB203580组对应时间点细胞凋亡减少 (P < 0.05),bax mRNA表达降低。说明细胞受到力学刺激会发生凋亡,而丝裂原活化蛋白激酶p38MAPK信号通路参与了该凋亡过程。

关键词: 丝裂原活化蛋白激酶, 周期性张应力, 凋亡, 成纤维细胞

Abstract:

BACKGROUND: When the teeth affected abnormal biting force, tooth absorption and periodontium would be greatly damaged.
OBJECTIVE: To study whether periodontal membrane fibroblast affected apoptosis following cyclic tensile stress stimulation and whether p38MAPK signaling pathway participated in apoptosis.
METHODS: Fibroblasts at passages from 4 to 7 were randomly assigned to control, loading and SB203580 groups after synchronization. In the loading and SB203580 groups, 12% strain was applied at a loading frequency of 6 cycles per minute, i.e. 5 seconds for tension and 5 seconds for relaxation. In the SB203580 group, cells were treated with 20 mmol/L p38MAPK inhibitor SB203580 at 1 hour before loading. At 6, 12 and 24 hours after loading, cells from each group were harvested, and cell apoptosis was detected using a flow cytometry. Expression of bax mRNA was determined using reverse transcription-polymerase chain reaction.
RESULTS AND CONCLUSION: Compared with the control group, apoptotic rate of fibroblasts and bax mRNA expression were increased after loading (P < 0.05), and enhanced over time, and peaked at 12 hour following loading, and then decreased gradually. Compared with the loading group, cell apoptosis was reduced at corresponding time points in the SB203580 group (P < 0.05), and bax mRNA expression was diminished. These results indicated that cells affected apoptosis after mechanics stimulation, and mitogen activated protein kinase p38MAPK signaling pathway participates in the process of apoptosis.

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